Evidence based practice guideline of chinese herbal medicine for psoriasis vulgaris

D'Arcy Little, MD, CCFP, Lecturer and Academic Fellow, Department of Family and Community Medicine, University of Toronto, ON. The need for relevant and timely information at the point of patient care is paramount in primary medicine. PDAs and Evidence-Based MedicineIt is important to note that the use of PDAs does not replace any of the steps involved in practising evidence-based medicine (EBM), but it may make some of them easier.
Barriers to Guideline ImplementationThe four-stage Pathman Model has been used to delineate the barriers that exist in guideline implementation.
Sackett and Straus have shown that the availability of a mobile "evidence cart"--consisting of EBM and medical reference material stored in laptops or paper inventories--in a busy inpatient medical service increased the extent to which evidence was sought and used in patient care decisions.13,14 However, the cart was found to be too bulky to take on bedside rounds. Because many of the studies describing the use of PDAs in implementing guidelines are continuing, often only descriptive reports are available. In the control and intervention phases, physicians collected data from 10 patient encounters for acute asthma. Patients in the intervention group tended to have a greater immediate clinical improvement, but this was not the case with intermediate term outcomes, which were similar between the groups. A prospective controlled pilot trial randomized family physicians to receive PDA software to help manage suspected angina or conventional care.
However, the actual guidelines that are chosen for implementation must be carefully selected. Acknowledgements: The author wishes to thank Laure Perrier of the Knowledge Translation Program at the Faculty of Medicine, University of Toronto, for assisting in some of the literature search for this article, and Dr. Table 1 reviews the steps devised by Straus and Sackett that are necessary to practice EBM.2 PDAs have the potential to make the best evidence available at the point of care in a fast and easily digestible format,6 thus facilitating steps 2, 3 and 4.
There is, however, one randomized trail suggesting that the use of PDAs can enhance guideline implementation.
During the intervention phase, PDAs provided structured documentation and offered recommendations based on the asthma guidelines of the American Academy of Pediatrics. Specifically, there was more measurement of peak expiratory flows and oxygen saturation, as well as increased administration of nebulized B-2 agonists and inhaled corticosteroids.
There were no differences in patient outcomes with respect to emergency room visits, hospitalizations or missed days of school at seven days post-visit. The software consisted of an algorithm that converts the patient's demographics, risk factors and findings into the probability of having coronary artery disease, and hence directs the clinician to the appropriate investigations and treatment. Sites are available that literally put evidence-based medicine in the hands of physicians at the point of care.
For example, several of the guideline steps in the Asthma study above, such as the administration of oxygen during an asthma exacerbation, are consensus statements without qualification of the evidence or the strength of the recommendations. Michelle Greiver for providing her abstract regarding the pilot trial of PDAs to help manage suspected angina. Effect of clinical guidelines on medical practice: a systematic review of rigourous evaluations. The horizon of continuing professional development: Five questions in knowledge translation. The personal digital assistant: a new medical instrument for the exchange of clinical information at the point of care.
A guideline implementation system using handheld computers for office management of asthma: effects on adherence and patient outcomes. Development and application of a generic methodology to assess the quality of clinical guidelines. Views and opinions in this publication and the website are not necessarily endorsed by or reflective of those of the publisher. The clinical genetics evolved from translational genetics research and contributes to the clinical care of patients and families through evidence-based health care in managing inherited disorders through accurate diagnosis, molecular pathology and assessing phenotypic correlations. Commonly used medical applications for PDAs include textbooks, rules and calculators, pharmacopoeias as well as scheduling and patient tracking programs. The software was found to increase overall use of cardiac stress testing, with a trend toward more appropriate use of stress testing. PDAs are a viable way to increase physician awareness of guidelines by allowing guideline programs to be easily downloaded and searched, and to increase physician adoption of and adherence to guidelines because the required information and reminders are close at hand and usable during patient encounters.
All guidelines, particularly those that are to be implemented on PDAs, should be rigorously assessed with respect to their scope and purpose, stakeholder involvement, rigour of development, clarity and presentation, applicability and editorial independence.18,19 Finally, the current lack of randomized controlled evidence for guideline implementation via the PDA will likely be remedied with time, as more such studies are completed and reported. Pilot randomized controlled trial of a new PDA-based software application for the diagnosis of suspected angina in primary care. Nine physicians enrolled 91 patients in the control phase and 74 patients in the intervention phase.
Gene mapping and deciphering pathogenic mutations have helped in unravelling the basic biological mechanisms leading to new drug discovery and development. Targeted pharmacotherapy is now possible for managing the highly penetrant multi-system dominantly inherited conditions. Notable examples include rapamycin (sirolimus) in suppressing the mTOR pathway associated hamartomas in dominantly inherited cancer family syndromes and angiotensin converting enzyme receptor blockers (ACE-RB) in preventing aortic dilatation in Marfan syndrome and related familial arteriopathies.
The translational genomic research is the essential prerequisite for developing sound evidence-based diagnostic, therapeutic and prognostic clinical protocols for the practice of personalised clinical medicine.
La genetica clinica rappresenta un'evoluzione della ricerca genetica traslazionale e contribuisce alla cura dei pazienti attraverso la gestione delle malattie ereditarie tramite diagnosi accurate, un approccio molecolare alle patologie e la valutazione delle correlazioni fenotipiche. La mappatura genetica e la decifratura delle mutazioni patogenetiche hanno contribuito a chiarire i meccanismi biologici di base che portano alla scoperta e allo sviluppo di nuovi farmaci. La farmacoterapia mirata è ora possibile per la gestione delle condizioni ereditarie ad alta penetranza. Esempi rilevanti includono il rapamycin (sirolimus) per la soppressione della via mTOR associata all'amartoma nelle sindromi oncologiche ereditarie dominanti e gli ACE inibitori, per la prevenzione della dilatazione aortica nella sindrome di Marfan e nelle arteriopatie familiari correlate.
La ricerca traslazionale genomica è il prerequisito essenziale per lo sviluppo di solidi protocolli evidence-based, terapeutici e di diagnosi clinica per la pratica della medicina personalizzata. This individual evidence is collated with the external evidence based on the outcome of a number of laboratory and imaging investigations.
The modern medicine evolved during the early 19thcentury and had to forcibly separate itself away from medieval practices that were largely influenced by several social, cultural and spiritual practices and beliefs. It is well known that several clinical applications did not stand the test of time as these were not properly evaluated through the process of adequately regulated translational process.
The translation of scientific discoveries into clinical practice and the discovery of population-level health benefit have always been slow and difficult. It is thus essential that the whole process of translational research is properly managed to ensure delivering reliable and clinically relevant outcomes. The whole process of the translational research includes four phases and revolves around the development of evidence-based guidelines (Figure 1). The process should be able to accommodate new knowledge that will inevitably arrive during translation research. Although evidence-based health practice is generally welcomed by clinicians, health professionals, health planners and health managers, it is not yet fully incorporated in all spheres of the medical and health profession.

One of the major hurdles is faced by clinicians on daily basis is selecting the best available evidence. It has been widely recognised that the clinical staff cannot be expected to undertake this evaluation themselves prior to undertaking clinical decisions across a busy practice. Increasingly, databases and information systems have been developed to provide topic-based summaries of research evidence which can be made available to health professionals. One of the established is the Cochrane Collaboration based in Oxford, England which now works with other international networks.
EGAPP seeks to establish an independent, systematic, evidence-based process for assessing genetic tests and other applications of genomic technology as these procedures transition from research to clinical and public health practice. This process yields summaries of the effectiveness of treatments and other interventions in particular fields of care. The widespread use and the availability of the Internet facilities are crucial in developing, teaching and promoting EBM.
These institutions and organisation can examine the evidence and prepare clinical guidelines that could be useful to clinicians and health commissioners. There are several clinically useful guidelines and protocols now available on the public domain of this institution that are regularly reviewed and updated.
The human body is organised into organ systems, tissues, cells, and cell components that are reduced to genetic and genomic profile. The structure-function relationship in biological terms is ultimately dependent upon the genotype.
The molecular dissection at the genome or gene level is thus fundamental to understanding the morbid variation in terms of anatomy, physiology and biochemistry. The scope of molecular and cell biology in medicine is unlimited as this encompasses practically whole of genetics and genomics.
Genetics conventionally relates to specific genes in relation to a number of different traits and characteristics whilst genomics encompasses the whole genome including all genes, DNA polymorphisms, RNA and its varied forms, and all other polymorphisms that might have current or evolutionary biological relationships. Thus it is not surprising to encounter plenty of evidence around in support of the role of genetics and genomics in the understanding of both normal structure and pathologic changes in relation to practically all aspects of clinical medicine ranging from the most uncommon disorders to the most common medical diseases that afflict the humans. The pharmacotherapeutic approach has always been the centre point of medical or even surgical treatments.
Even in ancient times, drug administration, whether in the form of herbal or mineral preparation or a combination, was tailored according to age, body size and gender. This concept is evolving and is now firmly established as tremendous progress has been made over several hundred years.
Medical practice now comprises health promotion and disease prevention and is on the verge of transformation as the scientific and medical communities move from evidence- based medicine to genomic medicine. Thus evidence that has now accumulated from the genomic research is plentiful and powerful in clarifying the biological understanding of a number of complex diseases. This information is now rapidly harvested in designing new diagnostic tools and as well as those in making pharmaco-therapeutic decisions and predicting the outcome. Gene expression studies using the microarray genomic technology have been used in defining the broad group distinctions as another mean to define traditional risk factors. However, this approach is less successful in making accurate predictions in individual patients due to considerable heterogeneity within these broadly defined groups.
This can be possibly resolved using multiple gene expression patterns and combining this with individual characteristics and predicting outcomes. Several disease groups have attracted the attention of researchers employing a number of genomic approaches.
In the treatment of cardiovascular disease the current strategies include relying on using a cocktail of drugs of proven efficacy.
In some cases, consideration of age, body size, gender and ethnic origin is taken into account in choosing the drug. Most patients benefit from only a few of the five or so drugs that are commonly prescribed. Although positive effects are seen in most, negative side effects are seen in some patients.
Undoubtedly the clinician would welcome any evidence-based approach in selecting the appropriate drug with the maximum efficacy and minimum side effects. It is often argued that in some cases the treatment selected is somewhat harsh and aggressive, and on the other hand in some cancers an aggressive approach should be adopted from start to achieve the best possible clinical outcomes.
For example, a woman diagnosed with early stage breast cancer will normally undergo surgery for removal of the tumour and then, typically, be treated with adjuvant chemotherapy.
It is possible that some of these women could be spared the harsh reality of chemotherapy should reliable tests for better longer-term clinical prediction be available.
Traditional clinical risk factors, such as tumour size, patient age, regional lymph node spread and estrogen receptor status are commonly used in predicting the disease progression and the prospects of recurrence. However, information derived from these parameters is often unreliable in identifying patients who will respond better with therapy from others who might end up with poor outcome and recurrences. In the same context, some patients might not require the unpleasant chemotherapy and could be spared from this and avoid unnecessary morbidity. Genomic information, in the form of gene expression profiles within tumour samples together with individual's genomic profile (SNPs and CNVs), has in recent years demonstrated the capacity to identify characteristics that reflect tumour behaviour and that relate to disease progression and outcomes, including cancer recurrence.
Tumour-based gene expression data from DNA microarrays adds immense detail and complexity to the information available from traditional clinical and pathological evidence. This approach has the potential to group breast cancer patients into high-risk and low-risk categories in the context of long-term recurrences. Patients categorised into high-risk would be likely to have more recurrences and long-term morbidity with probably higher mortality.
Whatever may be the argument in favour or against personalised medicine, this is what is expected by the patient and this is what every clinician is professed to deliver. Starting from the initial days of medical school, all medical students and trainee doctors are taught the art of clinical medicine that includes collecting details of patient's personal and past history in the context of relevant family and social history.
This is then put together in the context of presenting symptoms and signs and the outcomes of various radiological and laboratory investigations.
So what is different now, in particular following the completion of the human genome sequence and other advances in genome science and technology? All these parameters are intricately related and the outcome in the form of morbidity and health implications is individualised.
Essentially every individual carries the inherent biological predisposition to react or behave to a causative factor, the capacity to withstand the unwanted effects of the causative factor, making the best use of the available environmental factors including the pharmacological agents, and contributing to the prevention of progression of the particular disease or disorder. Both these specialist fields require a thorough understanding of functioning of genes, molecules, metabolic pathways and immunological processes.
The practice of medical or clinical genetics is exclusively confined to dealing with the diagnosis, the risk assessment and communication, and to some extent taking part in the management which is largely of preventive nature. This is probably more relevant in the context of microbial diseases where the knowledge of genomic profile of the pathogenic organisms (Pathogenomics) can be utilised in establishing the susceptibility or protective ability to the particular pathogen.
On the other hand genomic profiling can provide the evidence that the individual is more likely to positively or negatively respond to a particular anti-micobial agent.

These are also referred to as complex disorders, for example bronchial asthma, diabetes mellitus, coronary artery disease, bipolar depression and some common cancers. The individual genomic profiling, which is now possible with the use of variety of microarrays, can enable identification of individuals who are at higher risk of developing the disease and those who can receive bespoke advice on life-style modification, avoidance of contributing environmental factors, and institution of short-term and long-term pharmacotherapy. Mutations that change the function of genes encoding signalling proteins may result in a broad spectrum of human conditions ranging from birth defects to cancer.
In some Mendelian disorders the precise knowledge of mutations disrupting or modulating the signalling pathway has led to a better understanding of the underlying pathophysiology. In some cases this knowledge has now offered new opportunities to therapeutically manipulate signalling.
This section of the article briefly introduces this exciting development using two such examples.
Numerous mTOR mutations result in the hyperactivation of the signalling pathway and result in multiple tumours that comprise the phenotype of several uncommon Mendelian disorders with increased incidence of hamartomas and cancer (Figure 3). Inappropriate activation of mTORC1 has been demonstrated in the epithelium lining a proportion of renal cysts from human patients with ADPKD and in multiple rodent models. ADPKD is now an established ciliopathy where PC1 and PC2 localise to the primary cilia of renal epithelial cells. Several researchers are now engaged in gathering further evidence of mTORC1 activation in disorders associated with primary ciliary dysfunction.
However, another way of reducing TGFβ signalling is to target the angiotensin pathway with a small-molecule angiotensin II type 1 receptor blocker such as losartan, a widely used antihypertensive agent. The doses of losartan and propranolol were titrated to obtain comparable changes in blood pressure. Propranolol reduced the aortic root dilatation compared with placebo, but losartan completely inhibited aortic root dilatation, and losartan-treated animals were indistinguishable from wild-type controls. In light of these promising results, a number of clinical trials of losartan for Marfan syndrome have begun. Increased TGFβ activity has been implicated in the pathogenesis of the X-linked Duchenne (DMD) and (BMD) Becker muscular dystrophies, caused by mutations in the DMD gene. Early in the disease both muscle cell death and regeneration are seen, but regeneration slowly fails and fibrogenesis occurs. It is not always possible to provide a satisfactory distinction between a disease and disorder. On the other hand a disorder may involve more than one body systems or organs reflecting in sequence of patho-physiological events all leading to the morbid state. Thus for a disease or disorder to become apparent, there should be a significant disturbance in the body's internal environment or milieu interior.
The external factors that are capable for disturbing the internal metabolic environment include diet and microbial infection. The five decades of advances and developments in genetics have provided ample evidence for metabolic and molecular bases of human disease.
A number of genes, gene polymorphisms and genomic sequences of unknown functions govern the internal metabolic environment. Thus essentially almost all human disorders or diseases will have some form of direct or indirect genomic bases. But this is now discounted as several inherent factors are known to make an individual react in severe pathological manner to mild trauma whilst other person can withstand the impact of severe trauma, such as severe crush injury or burns. The broad term of pharmacogenomics has been used which is appropriately discussed along with pharmacogenetics. These two models are discussed in this review (see previous chapter "Targeted molecular therapy").
The purpose here is to revisit the scope of evidence-based medicine in the rapidly changing medical and health practices following the completion of human and other genomes. The new genome-based technologies and bioinformatics tools offer tremendous power for revolutionising the diagnosis and therapy in a number of human diseases.
The genome-based evidence, made accessible to clinicians and health professionals, is robust, accurate and individualised or narrowed down to the small patient population groups.
The future clinicians and health professionals will need to be equipped with knowledge and skills in applying broad range of genomic-based diagnostic and therapeutic tools. The transition from the present day conventional evidence-based approach to genomic-based evidence approach is in process leading to genomic medicine. The practice of evidence-based medicine including health promotion and prevention of disease, stands at a critical juncture as the scientific and medical community embrace itself with the rapidly expanding and revolutionising field of translational genomic research. What kind of evidence is it that evidence-based medicine advocates want health care providers and consumers to pay attention to? The continuum of translation research in genomic medicine: how can we accelerate the appropriate integration of human genome discoveries into health care and disease prevention? Towards integrated clinico-genomic models for personalized medicine: combining gene expression signatures and clinical factors in breast cancer outcomes prediction. Matching treatment to the genetic basis of (lipid) disorder in patients with coronary artery disease.
The role of a common variant of the cholesteryl ester transfer protein gene in the progression of coronary atherosclerosis. The Ile164 beta2-adrenergic receptor polymorphism adversely affects the outcome of congestive heart failure.
Targetting mtor-dependent tumours with specific inhibitors: a model for personalized medicine based on molecular diagnoses.
Davies DM, Johnson SR, Tattersfield AE, Kingswood JC, Cox JA, McCartney DL, Doyle T, Elmslie F, Saggar A, de Vries PJ, Sampson JR. Ravikumar B, Vacher C, Berger Z, Davies JE, Luo S, Oroz LG, Scaravilli F, Easton DF, Duden R, O'Kane CJ, Rubinsztein DC.
Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease. Altered transforming growth factor-beta signaling in a murine model of thoracic aortic aneurysm. Cohn RD, van Erp C, Habashi JP, Soleimani AA, Klein EC, Lisi MT, Gamradt M, Rhys CM, Holm TM, Loeys BL, Ramirez F, Judge DP, Ward CW, Dietz HC. Angiotensin II type 1 receptor blockade attenuates TGF-beta-induced failure of muscle regeneration in multiple myopathic states. Reading the metabolic fine print: The application of metabolomics to diagnostics, drug research and nutrition might be integral to improved health and personalized medicine.
On a medicine of the whole person: away from scientistic reductionism and towards the embrace of the complex in clinical practice.

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